The systemic hemodynamic actions of isoflurane (a volatile anesthetic) and etomidate and midazolam (intravenous anesthetics) have been well documented. However, few studies have investigated the actions of these agents on central cardiovascular control sites. The present investigation examined the actions of these agents on the responses of systolic arterial pressure (SAP), heart rate, infrarenal aortic blood flow, and lower body vascular resistance to central nervous system pressor site stimulation in chronically instrumented cats. Male and female cats (n = 23) were chronically instrumented with bipolar stimulating electrodes in the regions of the ventrolateral hypothalamus (anterior, 10.0 mm; lateral, 2.5 mm; depth, -4.0 mm) and mesencephalic reticular formation (anterior, 2.0 mm; lateral, 2.0 mm; depth, -1.0 mm). Control experiments consisted of stimulation sequences at 1x, 2x, and 4x threshold current levels to elicit pressor responses. Stimulation of the hypothalamic site produced current-dependent increases in SAP (6-85 mm Hg), in heart rate (3-56 beats/min), and in infrarenal aortic blood flow (0-85 mL/min). Reticular formation site stimulation produced graded increases in SAP (6-129 mm Hg) only. Isoflurane (1.5%, 2.5%, and 3.0%), etomidate (3.0-mg/kg bolus and 0.4-mg.kg-1.h-1 infusion), and midazolam (7.5-mg/kg bolus and 0.2-mg.kg-1.h-1 infusion) were then administered in separate experimental groups. After a steady hemodynamic state was established with each agent, stimulation sequences were repeated. Isoflurane produced an attenuation of the responses of SAP (from 85.1 +/- 8.2 to 17.8 +/- 6.1 mm Hg at 1.5%, to 7.2 +/- 2.0 mm Hg at 2.5%, and to 4.7 +/- 2.0 mm Hg at 3%, all P < 0.05), heart rate (from 41.1 +/- 13.0 to 12.5 +/- 2.7 beats/min at 2.5% and to 6.2 +/- 1.7 beats/min at 3%, all P < 0.05), and of the infrarenal aortic blood flow (from 72.6 +/- 14.3 to 11.8 +/- 4.2 mL/min at 1.5%, to 10.2 +/- 5.6 mL/min at 2.5%, and to 3.2 +/- 1.5 mL/min at 3%, all P < 0.05) to the highest level of hypothalamic site stimulation. Isoflurane similarly produced an attenuation of the SAP response (from 128.7 +/- 10.3 to 15.4 +/- 8.1 mm Hg at 1.5%, to 0.2 +/- 1.1 mm Hg at 2.5%, and to 0.3 +/- 0.5 mm Hg at 3.0%, all P < 0.05) to the highest level of reticular formation site stimulation. Etomidate administration attenuated SAP responses to the highest level of hypothalamic site stimulation (from 50.6 +/- 6.8 to 24.4 +/- 10.8 mm Hg, P < 0.05) and to the highest level of reticular formation site stimulation (from 92.7 +/- 14.0 to 23.8 +/- 12.6 mm Hg). Heart rate and blood flow responses were not changed by etomidate. Similarly, midazolam administration blunted the SAP responses to the highest level of hypothalamic site stimulation (from 73.0 +/- 8.9 to 38.0 +/- 7.2 mm Hg, P < 0.05) and to the highest level of reticular formation site stimulation (from 108.0 +/- 17.9 to 54.7 +/- 17.7 mm Hg, P < 0.05). Blood flow responses were not changed by midazolam, and only heart rate change at the highest level of hypothalamic stimulation was decreased (from 56.7 +/- 7.9 to 32.0 +/- 6.4 beats/min, P < 0.05). During emergence from isoflurane, occasional conversion of pressor to depressor responses was observed. The results suggest that disruption of central nervous system cardiovascular control centers may contribute to the alterations in hemodynamic stability produced by these anesthetic agents.
